Results 171 to 180 of about 190,698 (290)

TP53 Loss Elevates NF‐κB‐IFN‐β‐MHC‐Ia Signaling to Promote NK Cell Resistance in Osteosarcoma

open access: yesAdvanced Science, EarlyView.
TP53 loss in a transforming or osteosarcoma cell promotes cytosolic DNA accumulation, activating NF‐κB‐dependent IFN‐β production. Autocrine IFN‐β signaling increases cell‐surface HLA‐Ia expression, strengthens inhibitory KIR signaling in natural killer cells, and thereby enables the affected cell to evade NK cell‐mediated cytotoxicity.
Guihui Qin   +9 more
wiley   +1 more source

Multi‐Tissue Crosstalk Regulating Meniscus Healing Under Inflammation and Physiological Loading

open access: yesAdvanced Science, EarlyView.
Using a novel Meniscus‐on‐a‐chip (MoC) model integrated with a meniscus‐specific bioreactor, this study investigated the roles of multi‐tissue crosstalk that regulates injury, healing, and degeneration of the meniscus injury under inflammation and pathophysiological loading.
Hun Jin Jeong   +5 more
wiley   +1 more source

SAV1 in Cooperation With FKBP52 Participates in Implantation

open access: yesAdvanced Science, EarlyView.
The MST‐SAV1 complex modulates FKBP52 phosphorylation to fine‐tune PR activity, ensuring timely uterine transition to receptivity under estrogen signaling for implantation. Stromal SAV1 scaffolds MST1/2‐mediated FKBP52 phosphorylation via noncanonical Hippo to promote PR activity.
Yuhan Shao   +10 more
wiley   +1 more source

Nuclear IDH3A Drives Transcriptional Programs in Melanoma via the YBX1–JUN/FOS Axis

open access: yesAdvanced Science, EarlyView.
Genomic amplification drives aberrant nuclear localization of IDH3A in melanoma. Independent of its canonical metabolic activity, nuclear IDH3A cooperates with YBX1 to activate the c‐JUN/c‐FOS transcriptional program, while NONO facilitates its nuclear localization.
Juan Ran   +10 more
wiley   +1 more source

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